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Keith Jerome, who recently received one of the Grand Challenges Explorations grants from the Bill & Melinda Gates Foundation, looks over his notes in the research lab he manages at the Fred Hutchinson Cancer Research Center.

Keith Jerome has one year to spend $100,000.

But the UW associate professor of laboratory medicine isn’t going to buy a new car. He is going to use his grant from the Bill & Melinda Gates Foundation to try to find a cure for HIV.

“I think this is an important problem and we have a chance to really make a difference,” Jerome said.

The grant is part of the Grand Challenges Explorations grant program that includes a $100 million fund distributed during five years for research of health issues affecting the global community.

“It is part of the Grand Challenges in Global Health Initiative, which is supported by the Gates Foundation to achieve major breakthroughs in global health,” Gates Foundation member Becky Meisels said.

However, these grants are not given to just any researcher.

“The grants are given to researchers working on novel and potentially ground-breaking ideas that are off the beaten path,” Jerome said.

Jerome’s plan involves a new class of protein called homing endonucleases, proteins that are able to recognize and cut up specific sequences in DNA. He wants to change the specificity of these proteins so they can recognize the viral part of the DNA and then can introduce that into a person that has HIV. The idea came to him a little more than a year ago.

“The thing that makes HIV such a bad disease is that it actually put itself in your chromosomes,” Jerome said.

The current HIV treatments available cannot target the part of the virus that has integrated itself into the chromosome.

Jerome has worked with viruses for a long time, including work on the herpes virus, which is very similar to the HIV virus in that both viruses permanently inhabit the body.

“The idea really first came about generically when we were thinking about the latent viruses,” Jerome said.

The Gates Foundation helped jumpstart the idea into an actual plan.

“The one thing I would say is that for all of us who have gotten these Gates awards, I think there is a tremendous gratitude to the foundation for this,” Jerome said.

He added that during such a tough time in the economy, it is amazing to have this foundation as a source of funding.

The $100,000 grant Jerome received is for one year. At the end of the year, the foundation will look at the progress and re-evaluate the project. In the world of science, a year isn’t a very long time and it’s barely enough time to see if the ideas will work or not.

“At the end of the year, hopefully we will find funding to continue,” Jerome said.

The Gates Foundation has identified 12 areas as “grand challenges” that affect the world. Studies on an HIV cure is one of those areas.

“I applied for that one and basically our approach is a new way that offers the possibility of a cure for people with HIV,” Jerome said. “Not just a treatment, but a way to get the virus out of the body.”

Study Identifies Foothold Behind HIV Brain AssaultScientists have uncovered a number of events that take place after brain cells are infected by HIV, a virus whose assault on the nervous system continues unabated despite antiviral medications.

Researchers from the University of Rochester Medical Center and other institutions say that they have been successful in reversing the effects of Tat, a protein that is central to HIV's attack on cells called neurons, in the laboratory.

The scientists attribute their success to the discovery of the receptor that Tat uses to attack neurons. They say that it was by blocking this receptor that they could reverse the effects of Tat.

Writing about their work in the journal PloS One, the team insist that their work opens up a new avenue for exploring ways to prevent or treat HIV's neurological effects, for which there is no currently approved treatment.

Funded by the National Institute of Mental Health, the latest research project aims at finding out the first treatment for the neurological effects of HIV, known collectively as neuroAIDS or HIV dementia.

Dr. Harris Gelbard, a neurologist at the University of Rochester Medical Center, has revealed that Tat works through the ryanodine receptor to sicken neurons in two ways: by destroying the ability of mitochondria to protect themselves from changes in levels of calcium, and by affecting an organelle known as the endoplasmic reticulum, where proteins are actually assembled and folded.

The researcher says that it is Tat's effects on the ryanodine receptor that cause an "unfolded protein response" seen in the brains of HIV patients.

Gelbard says that the new findings are in line with past studies that showed that the central problem in HIV dementia is not that brain cells simply die, but rather they become sick and lose their ability to communicate with each other.

Since the cells are still alive, according to Gelbard, there is hope that the condition could be stopped or even reversed with proper treatment.

The researcher has revealed that the team were able to stop the harmful effects of Tat in neurons from mice by using the drug dantrolene, which blocks the ryanodine receptor.

Gelbard, however, cautions that dantrolene has side effects and thus may not be appropriate for use in people.

"A lot of people are under the impression that HIV has been 'solved,' that somehow, it's no longer a problem. But the disease never went away, and it's a huge problem," said Gelbard, who is professor of Neurology, Pediatrics, and Microbiology and Immunology.

"There are a fair number of similarities between this brain disease and other diseases, such as Parkinson's or Alzheimer's. We hope that what we are learning can be applied to other diseases as well," the researcher added.

Sorry for this bad news and this young guy.This work is dedicated to the nice young patient who courageously participated in this therapeutic proposal.

One of the challenges in HIV infection is viral eradication, as underlined by recent studies [1]. Allogeneic bone marrow transplantation (BMT) has been suggested to be able to reconstitute patients' haematopoietic systems after the clearance of HIV-infected cells with intensive chemotherapy and radiation [2,3]. In 1999, Huzicka [3] reviewed 32 allogeneic bone marrow transplants in HIV-infected patients between 1982 and 1996; in two cases, HIV seemed to be eradicated as judged by negative HIV-DNA and HIV-RNA levels using classic polymerase chain reaction [4,5].

We report here the first case of BMT in an HIV-1-infected patient treated by HAART. To explore HIV reservoirs, we used a sensitive method to quantify HIV-DNA levels in peripheral blood mononuclear cells (PBMC) and biopsies.

A Romanian 17-year-old man had a transfusion-related HIV-1 infection diagnosed at 8 years of age. He was asymptomatic with a CD4 cell count greater than 350 cells/_l until he developed Burkitt's lymphoma in June 2003 and then received effective HAART. He developed monocytic acute myeloid leukemia in April 2005. After transiently effective chemotherapy (ELAM02), a relapse occurred in September and a second line of chemotherapy followed by a human leukocyte antigen phenoidentical BMT was proposed in October. Marrow cytoablation consisted of a conditioning regimen including idarubicine, fludarabine and aracytine. Horse antilymphocytic serum and cyclosporine were used. Haematological restoration was observed at day 19 posttransplant, and chimerism study showed a 100% donor phenotype at days 30 and 119 posttransplant. Cytogenetic remission was confirmed on bone marrow at day 124. The patient suffered early and prolonged cutaneous and digestive graft-versus-host disease (grade III) partly controlled with a combination of immunosuppressive therapy. He presented with several infectious complications and died in multivisceral failure at day 191 posttransplant. During all the procedures, HAART was maintained except for a short interruption for suspected toxicity between days 114 and 134 posttransplant.

HIV DNA was quantified in PBMC, bone marrow cells and biopsies, using a real-time polymerase chain reaction assay amplifying the LTR region according to a previously described technique [6]. The lowest threshold possible was obtained and was adapted to each sample even in cases with few cells during the aplastic and immunosuppressive phases, because the maximum tests per sample were performed to explore all available cells. Before transplantation, HIV DNA was at 2.76 log10 copies/106 PBMC. The medullar sample was at 1.77 log10 copies/106 bone marrow cells before BMT; it contained 60% monoclonal blasts, suggesting that blasts were not infected otherwise the HIV-DNA load would have been dramatically higher. The plasma HIV-RNA load (Cobas Monitor; Roche, France) was undetectable for 18 months before BMT. After BMT, HIV RNA in the plasma remained at less than 1.7 log10 copies/ml. HIV-DNA levels in PBMC became undetectable during over 4 months (< 2 log10 copies/106 PBMC), although more than one million PBMC was explored (Fig. 1). Sixteen days after HAART cessation, however, rebounds of HIV RNA (4.61 log10 copies/ml) and HIV DNA (2.50 log10 copies/106 PBMC) were detected (Fig. 1). Resumption of HAART at day 134 returned viral loads to undetectable levels at day 152 (Fig. 1). HIV DNA was still detectable (< 1.5-2.5 log10 copies/106 PBMC; Fig. 1) but was undetectable in oesophageal, antral, duodenal and rectal biopsies performed 12 days after HAART resumption (< 2.3-3.3 log10 copies/106 cells).

We performed a phylogenetic analysis based on the gp120 C2-V3 sequences on four plasma viral strains (two in 2003 and two in 2006 after BMT). They clustered together but two separate lineages were identified (one for the strains of 2003 and one of 2006) with a high bootstrap value (> 95), suggesting that different quasispecies circulated before and after BMT. It confirmed that the viral reservoir previously constituted was not eradicated.

Negative results on HIV DNA after BMT gave hope of a significant reduction of the reservoir, indeed HIV remission. The organism was repopulated by donor-derived cells that could mount a successful antiviral response through cytotoxic T lymphocytes [3]. Moreover, graft-versus-host disease could have destroyed residual haematopoietic cells potentially harbouring virus [5], including infected macrophages [3]. We did not, however, observe HIV-1 eradication. Unfortunately, the HIV-1 replication recovery a few days after HAART interruption unambiguously showed the persistence of an infectious viral residual reservoir, may be in profound tissues. Despite the use of intensive pretransplant cytoablative conditioning with chemotherapy combined with 18 months of potent effective HAART before BMT (contrary to zidovudine alone used in cases described before 1996), the goal of HIV eradication was not achieved for this patient with a relatively high HIV-DNA level in PBMC [6]. We hypothesized that recipient antigen-presenting cells as well as totipotent haematopoietic progenitors can survive and play a critical role as a virus reservoir [7-9]. Finally, this case emphasizes that the establishment of an 'eradication concept' needs to be evaluated after HAART cessation.

Raltegravir Clinical Efficacy Against B Subtype and Non-B Subtype HIV-1 is SimilarBased upon data available from 3 randomized clinical trials, raltegravir exhibitscomparable antiviral clinical activity against B and Non-B HIV-1 infection in treatment naive patients up to 96 weeks and in treatment experienced patients up to 48 weeks.Resistance mutations that arise at failure for Non-B viruses are similar to those observed previously, specifi cally at positions N155H and Y143R

Better CD4 Gains on Antiretrovirals Linked to Clearance of Cancer-Causing HPVA significantly higher percentage of human papillomavirus (HPV)-infected women with higher CD4 counts during follow-up (usually on antiretroviral therapy) cleared their HPV infection, according to results of Belgian HPV screening study that involved a high proportion of women born in Africa. As in earlier studies, younger age and a lower CD4 count correlated with higher HPV prevalence. HPV can cause cervical cancer, an AIDS-defining cancer. Women with HIV run a higher risk of cervical cancer despite the advent of potent antiretroviral.

Risks and Benefits of 5 Days On/2 Days Off in the FOTO StudyPeople who took a weekend break from their regimen of efavirenz, tenofovir (TDF), and emtricitabine (FTC) made it through a 24-week study with the same viral control rate as people who took those antiretrovirals 7 days a week. This small, intriguing trial took a novel slant on the goals of planned treatment interruptions.

No Evidence of Virologic Benefit With Higher Lopinavir Dose for ChildrenA higher lopinavir/ritonavir dose, preferred by certain pediatricians because some evidence suggests a virologic benefit over a lower recommended dose, yielded no response advantage in an analysis of 160 children in the UK/Irish Collaborative HIV Paediatric Study (CHIPS) [1]. Guidelines call for a target total daily dose of 460 mg/m(2) of ritonavir-boosted lopinavir for children taking the protease inhibitors (PIs) without a nonnucleoside and 600 mg/m(2) for children taking the PIs with a nonnucleoside. But some pediatricians aim for the 600 mg/m(2) target even without a nonnucleoside because of a perceived antiviral advantage with the higher dose.

More Time With Sub-500 Load on First Regimen Cuts Risk of Second-Line FailureKeeping HIV under control longer with a first antiretroviral combination trimmed the risk of second-line failure in people whose first regimen eventually did falter, according to results of a 1917-person EuroSIDA analysis [1]. Time to initial viral suppression, total time with a sub-500-copy load, number of rebounds, and rebound size did not predict second-line failure in this study. Research shows that numerous factors predict response to combination antiretroviral therapy (cART), including resistance, adherence, toxicity, pretreatment viral load and CD4 count, and treatment with suboptimal regimens. But until this analysis, no one had systematically addressed the impact of first-line viral suppression patterns on future virologic failure.

Lipid effects in the ARTEMIS and TITAN trials: effects of demographics, HIV disease stage, treatment arm and lipid-lowering drugsRises in lipid parameters during the ARTEMIS and TITAN trials were influenced by several factors. In the ARTEMIS trial, older patients tended to have larger rises in Total cholesterol and triglycerides. Baseline CD4 cell counts and HIV RNA levels were not associated with changes in lipids during this trial.In both trials, DRV/r led to significantly smaller rises in Total cholesterol, HDL and triglycerides than LPV/r. The ratio of Total cholesterol/HDL remained stable over time in both treatment groups, for both trials.In the TITAN trial, patients using EFV or NVP showed significantly greater rises in Total cholesterol, HDL and triglycerides.In each trial, including or excluding data on lipid-lowering drugs had no effect on estimates of mean change in lipids over time.

10 Nov 2008 - Bavarian Nordic has completed a clinical safety report from a large Phase II study with IMVAMUNE in HIV infected subjects that confirms the excellent safety profile of IMVAMUNE. Within the next few days the safety report of this study will be submitted to the FDA and this will trigger a USD 25 million milestone payment under the RFP-3 contract. The clinical safety report constitutes a major part of the data package that will be used to potentially support the use of IMVAMUNE in a declared emergency.

In support of using IMVAMUNE as a smallpox vaccine in individuals otherwise contraindicated to receive conventional vaccinia vaccines, Bavarian Nordic has performed a large Phase II study in HIV infected subjects with CD4 counts between 200 and 750 cells/µl to compare the safety to healthy subjects.

The safety report from this study, which represents an essential part of the EUA data package, includes safety data from over 300 HIV infected and 86 healthy subjects, all of whom had no history of prior smallpox vaccination. The low number of adverse events confirmed the favourable safety profile of IMVAMUNE in vaccinia-naïve HIV infected subjects with varying degrees of immune suppression. Indeed, there was no difference in adverse events between the healthy and HIV infected subjects, even in the most immune compromised patients (CD4 counts >= 200-350 cells/µl). IMVAMUNE has now been tested in more than 2,200 people in 11 completed or on-going clinical studies, which includes a large proportion (more than 750) of immune-compromised people i.e. HIV infected or diagnosed with Atopic Dermatitis (AD) who are excluded from vaccination with traditional smallpox vaccines.

The complete data set from this trial is expected to be reported in the second half of 2009. The final report will include data on immunogenicity as well as long-term (6-month) safety information and will contain data from subjects enrolled in an additional study arm funded by the NIH under RFP-2 (HIV infected subjects with a history of previous exposure to a conventional smallpox vaccine).

Bavarian Nordic receives USD 25 million milestone payment after submission of IMVAMUNE data to the U.S. Health Authorities

21 Nov 2008 - Bavarian Nordic has invoiced the U.S. authorities for another milestone payment of USD 25 million as allowed under the RFP-3 contract to manufacture and deliver 20 million doses of the company's IMVAMUNE smallpox vaccine. This milestone payment was triggered by the recent submission of a clinical safety report from a large Phase II study with IMVAMUNE in HIV infected subjects, which is part of the regulatory package that will be used to potentially support the use of IMVAMUNE in a declared emergency. With this, Bavarian Nordic is an important step closer to fulfilling the conditions for initiating delivery of IMVAMUNE in 2009.

With this payment, Bavarian Nordic has so far invoiced a total of USD 125 million in advance- and milestone payments under the RFP-3 contract, of which USD 50 million has not yet been recognised in the income statement.

Anders Hedegaard, President & CEO of Bavarian Nordic, said: "Since the award of the RFP-3 we have successfully met all agreed objectives in the contract with the U.S. Department of Health and Human Services and we find this very satisfactory. The submission of these clinical data concludes the data package that may support the use of IMVAMUNE in a declared emergency and marks an important event for the company this year. This submission is part of the company's plan to support the delivery of IMVAMUNE which is planned to start during 2009".

CD4 cell counts of 800 cells/mm3 or greater after 7 years of highly active antiretroviral therapy are feasible in most patients starting with 350 cells/mm3 or greater.

Objective: CD4 cell count changes in therapy-naive patients were investigated during 7 years of highly active antiretroviral therapy (HAART) in an observational cohort.

Methods: Three endpoints were studied: (1) time to ≥800 CD4 cells/mm3 in 5299 therapy-naive patients starting HAART, (2) CD4 cell count changes during 7 years of uninterrupted HAART in a subset of 544 patients, and (3) reaching a plateau in CD4 cell restoration after 5 years of HAART in 366 virologically suppressed patients.

Results: Among patients with <50, 50 to 200, 200 to 350, 350 to 500, and ≥500 CD4 cells/mm3 at baseline,

Periods with HIV RNA levels >500 copies/mL and age ≥50 years were associated with lesser increases in CD4 cell counts between 6 months and 7 years. Having reached ≥800 CD4 cells/mm3 at 5 years, age ≥50 years, and ≥1 HIV RNA measurement >1000 copies/mL between 5 and 7 years were associated with a plateau in CD4 cell restoration.

Conclusions: Restoration to CD4 cell counts ≥800 cells/mm3 is feasible within 7 years of HAART in most HIV-infected patients starting with ≥350 cells/mm3 and achieving sufficient suppression of viral replication. Particularly in patients ≥50 years of age, it may be beneficial to start earlier than current guidelines recommend.

A new vaccine principle is being developed by scientists at the University of Copenhagen which – if it works to its full expected potential – could help to save millions of lives and revolutionise current vaccine technology. The ‘InVacc’ platform, as it is known, represents an advance on the original DNA vaccines and generates new vaccines with greatly enhanced properties.

The platform consists of a chain of amino acids attached to a gene of the virus being vaccinated against. This genetic cocktail is then inserted into an incapacitated flu-like virus such as the adenovirus and injected into the body, where it triggers a broader and more aggressive immune response, enabling the immune system to quickly seek out and destroy the disease when it invades.

“We are excited to be working on the vaccine technology”, says Associate Professor Jan Pravsgaard, the lead scientist behind the project. “The platform has proved very effective in our recent tests and could have enormous potential. In principle, vaccines of this type could be used to inoculate against a range of deadly viruses, bacteria and other disease-causing agents and even be used to cure certain cancers once they take hold.”

Tests of the vaccine platform on mice so far look extremely promising with the scientists able to provide 100% protection against different, lethal strains of flu given to the test animals.

The scientists also believe that the new technology will be effective despite the ability of different viruses and bacteria to constantly mutate and develop resistance.

Key benefits of the new technology:

* The new platform delivers a broad and very powerful immune response, enabling the immune system to defeat invading pathogens. * Unlike many vaccines, InVacc activates the CD4+ T cells of the immune system, which govern and coordinate the other immune system attack cells. For reasons not yet fully understood, activating the CD4+ cells enhances the response of the associated attack cells (producing large numbers of CD8+ cells) and is an important rea-son why the platform is able to deliver such a strong immune response. * InVacc provides rapid protection. In animal tests, complete pro-tection was achieved in less than 3 days after a single vaccination. This could have significant implications for the handling of epidemics, quickly halting infection rates and preventing major outbreaks.

The Scandinavian company Novo A/S and the Novo Nordisk Foundation have such faith in the new technology that they have already invested funds to create a strategic plan for development and use of the platform. “The grants awarded through our Novo Seeds programme are only for very select projects that show outstanding promise, both scientifically and commercially, explains Novo Seeds Investment Director, Stephen Christgau.” “The InVacc platform is definitely one of those. Our grants will help the team to develop and commercialise their groundbreaking research and validate the advantages of the vaccine platform against competing technologies”.

HIV infections hit record high• Estimated 77,400 people had the virus last year, HPA says• Call for wider testing as quarter remain unaware of infection

The Guardian (UK)

Record numbers of people in the UK are living with HIV, with more than half of newly diagnosed infections found in heterosexuals, figures revealed today.

The Health Protection Agency (HPA) said that in 2007 an estimated 77,400 people had the virus, up from 73,000 in the previous year. More than a quarter of those infected remained unaware of their status.

During 2007, 7,734 new cases of HIV were found, including in 3,160 gay men and 4,260 heterosexual men and women.

The estimated number of people infected through heterosexual contact in the UK jumped from 540 in 2003 to 960 in 2007, figures show.

Almost a third of people who found out they were infected were diagnosed late, at a point after which treatment should have begun. They risked losing benefits associated with early diagnosis, including prolonged life expectancy.

Valerie Delpech, the head of HIV surveillance at the HPA's Centre for Infections, said: "Diagnosing HIV infections earlier will reduce transmission of this infection as those unaware of their positive status pose a greater risk to future sexual partners. Late diagnosis also has a major impact on disease and life expectancy and it is vital that people are diagnosed early.

"It is worrying that so many people remain unaware of their HIV status. Wider HIV testing in high prevalence areas of the UK is urgently needed to reduce the number of undiagnosed infections."

Lisa Power, head of policy at the HIV charity Terrence Higgins Trust, said: "There are now well over 20,000 people in the UK who have HIV and don't know it. Not only is this dangerous to their own health, but they are more likely to pass the virus on than someone who has been diagnosed."

New guidelines recommend wider HIV testing in areas of the country where the prevalence of the virus is greatest, such as London, Manchester and parts of the south coast.

Delpech said: "Access to testing must be made easier. We need to improve availability of HIV testing in a number of healthcare settings, including general practice, to improve diagnosis of this infection. Without this we will not see the reduction in transmission that we need to see, or a further fall in serious disease."

Peregrine Pharmaceuticals Awarded Broad New U.S. Patent for Anti-Viral Applications of Phospholipid-Targeting Antibodies

Peregrine Pharmaceuticals, Inc. , a clinical stage biopharmaceutical company developing monoclonal antibodies for the treatment of serious viral infections and cancer, today announced that the U.S. Patent and Trademark Office has issued U.S. Patent Number No. 7,455,833, which includes broad claims covering anti-viral applications of antibodies that directly bind to aminophospholipids.

The aminophospholipid family of phospholipids, including phosphatidylserine (PS), represents a novel target for anti-viral therapies. The new patent follows publication this week of a study in Nature Medicine that supports the broad anti-viral potential of the company's anti-phospholipid platform, showing that phospholipid-targeting drugs can cure lethal virus infections in animal disease models

..

PS is a lipid molecule usually found on the inside of cell membranes that "flips" and becomes exposed on the outside of the membranes of virally infected cells and enveloped viruses. Exposed PS is known to be immunosuppressive and could potentially enable viruses to evade immune recognition. By masking the exposed PS, Peregrine's antibodies may block these immunosuppressive signals and allow the body to develop a robust immune response to the viral pathogen. Anti-PS antibodies have been shown to help clear infectious virus from the bloodstream and to induce antibody-dependent cellular cytotoxicity, an important anti-viral immune response. Researchers have found that PS is exposed on the outer membrane of cells infected with HIV, influenza, hemorrhagic fever viruses, CMV, herpes simplex viruses and smallpox viruses.

In addition to its potent anti-viral activity in lethal viral disease models, Peregrine's anti-PS antibody bavituximab appeared safe and well tolerated with promising signs of anti-viral activity in Phase I trials in patients with chronic HCV infection. Based on these positive data, Peregrine has initiated a trial in patients co-infected with HCV and HIV, a population that in the U.S. includes about 30% of all HIV patients.

The above patent is part of the anti-ps therapy that Peregrine Pharm is working on in conjunction with CHAVI. It's peregrine's mabs that Duke university is working with to produce both a cure and a vaccine.Bavituximab, as stated, has already been in clinical trials with top line safety data in over 100 patients in phase 1 and phase 2 has already started for cancer indications. Results of the hepc/hiv trial will be released in the first half of 2009. I believe CHAVI will have something to report sooner. This therapy is very promising and potentially could be the HOLY GRAIL. Nowhere else have I heard the cure word expressed with an hiv therapy as was said by some of the most respected hiv researches in the world. I also don't think CHAVI would be involved with anti-ps if they hsdn't noticed something wonderful (adaptive immunity). The wait is stomach turning and I for one would try this therapy tomorrow if it were available.

A new game, named Foldit, turns protein folding into a competitive sport. Introductory levels teach the rules, which are the same laws of physics by which protein strands curl and twist into three-dimensional shapes -- key for biological mysteries ranging from Alzheimer's to vaccines.

After about 20 minutes of training, people feel like they're playing a video game but are actually mouse-clicking in the name of medical science. The free program is at http://fold.it/.

The game was developed by doctoral student Seth Cooper and postdoctoral researcher Adrien Treuille, both in computer science and engineering, working with Zoran Popovic, a UW associate professor of computer science and engineering; David Baker, a UW professor of biochemistry and Howard Hughes Medical Institute investigator; and David Salesin, a UW professor of computer science and engineering. Professional game designers provided advice during the game's creation.

"We're hopefully going to change the way science is done, and who it's done by," said Popovic, who presented the project today at the Games for Health meeting in Baltimore. "Our ultimate goal is to have ordinary people play the game and eventually be candidates for winning the Nobel Prize."

Proteins, of which there are more than 100,000 different kinds in the human body, form every cell, make up the immune system and set the speed of chemical reactions. We know many proteins' genetic sequence, but don't know how they fold up into complex shapes whose nooks and crannies play crucial biological roles.

Computer simulators calculate all possible protein shapes, but this is a mathematical problem so huge that all the computers in the world would take centuries to solve it. In 2005, Baker developed a project named Rosetta@home that taps into volunteers' computer time all around the world. But even 200,000 volunteers aren't enough.

"There are too many possibilities for the computer to go through every possible one," Baker said. "An approach like Rosetta@home does well on small proteins, but as the protein gets bigger and bigger it gets harder and harder, and the computers often fail.

"People, using their intuition, might be able to home in on the right answer much more quickly."

Rosetta@home and Foldit both use the Rosetta protein-folding software. Foldit is the first protein-folding project that asks volunteers for something other than unused processor cycles on their computers or Playstation machines. Foldit also differs from recent human-computer interactive games that use humans' ability to recognize images or interpret text. Instead, Foldit capitalizes on people's natural 3-D problem-solving skills.

The intuitive skills that make someone good at playing Foldit are not necessarily the ones that make a top biologist. Baker says his 13-year-old son is faster at folding proteins than he is. Others may be even faster.

"I imagine that there's a 12-year-old in Indonesia who can see all this in their head," Baker says.

Eventually, the researchers hope to advance science by discovering protein-folding prodigies who have natural abilities to see proteins in 3-D.

"Some people are just able to look at the game and in less than two minutes, get to the top score," said Popovic. "They can't even explain what they're doing, but somehow they're able to do it."

The game looks like a 21st-century version of Tetris, with multicolored geometric snakes filling the screen. A team that includes a half-dozen UW graduate and undergraduate students spent more than a year figuring out how to make the game both accurate and engaging. They faced some special challenges that commercial game developers don't encounter.

"We don't know what the best result is, so we can't help people or hint people toward that goal," Popovic explained. The team also couldn't arbitrarily decide to make one move worth 1,000 bonus points, since the score corresponds to the energy needed to hold the protein in that shape.

Almost 1,000 players have tested the system in recent weeks, playing informal challenges using proteins with known shapes. Starting this week, however, the developers will open the game to the public and offer proteins of unknown shapes. Also starting this week, Foldit gamers will face off against research groups around the world in a major protein-structure competition held every two years.

Beginning in the fall, Foldit problems will expand to involve creating new proteins that we might wish existed -- enzymes that could break up toxic waste, for example, or that would absorb carbon dioxide from the air. Computers alone cannot design a protein from scratch. The game lets the computer help out when it's a simple optimization problem -- the same way that computer solitaire sometimes moves the cards to clean up the table -- letting the player concentrate on interesting moves.

Eventually, the researchers hope to present a medical nemesis, such as HIV or malaria, and challenge players to devise a protein with just the right shape to lock into the virus and deactivate it. Winning protein designs will be synthesized in Baker's lab and tested in petri dishes. High-scoring players will be credited in scientific publications the way that top Rosetta@home contributors already are credited for their computer time.

"Long-term, I'm hoping that we can get a significant fraction of the world's population engaged in solving critical problems in world health, and doing it collaboratively and successfully through the game," Baker said. "We're trying to use the brain power of people all around the world to advance biomedical research."

Foldit includes elements of multiplayer games in which people can team up, chat with other players and create online profiles. Over time the researchers will analyze people's moves to see how the top players solve puzzles. This information will be fed back into the game's design so the game's tools and format can evolve.

New Antibiotic Against Serious InfectionsBeerse, Belgium (November 21, 2008) - The Committee for Medicinal Products for Human Use (CHMP) has recommended approval for the antibiotic, ZEVTERA(TM) (ceftobiprole medocaril) for the treatment of complicated skin and soft tissue infections. The CHMP's positive opinion is now referred for final action to the European Commission.

Ceftobiprole is the first, broad-spectrum, anti-MRSA cephalosporin antibiotic with activity against a range of difficult-to-treat Gram-positive and Gram-negative hospital- and community-acquired infections including methicillin-resistant Staphylococcus aureus (MRSA) and Pseudomonas aeruginosa.

In clinical trials, ceftobiprole has demonstrated high cure rates in patients with complicated skin infections, including those with deep wound and diabetic foot infections, and in infections caused by the potentially deadly MRSA.

The use of ceftobiprole in adults for the treatment of complicated soft tissue infections is under regulatory review in the United States, and Australia, among other countries. Ceftobiprole was approved in Switzerland in November 2008. In Canada, it was approved and launched in August 2008, and is marketed under the trade name ZEFTERA.

ETR has been used with a wide range of ARVs in the early access programme in Europe

In the overall cohort (N=941), the percent of patients with HIV RNA <50 copies/mL increased from 15% at baseline to 74% at Week 24 (observed data)

In a pre-planned substudy, the cohort of 176 patients who took ETR, DRV/r and raltegravir showed strong efficacy - 93% had HIV RNA levels below 400 copies/mL by Week 24, with 70% showing HIV RNA <50 copies/mL at this time

It is difficult to reliably evaluate efficacy by use of different ARVs in the early access cohort, since baseline drug resistance data is not available and there is minimal data collection in this very diverse patient population

Among patients with virological rebound, a significantly lower proportion of ETR-treated patients showed development of DRV RAMs compared with placebo-treated patients

Among patients with virological rebound and DRV FC In the DUET studies, adding ETR to a DRV/r containing regimen protects the activity of DRV/r in cases of virological rebound in HIV-1-infected, highly treatment-experienced patients with existing PI resistance at baseline

Among patients with virological rebound, a significantly lower proportion of ETR-treated patients showed development of DRV RAMs compared with placebo-treated patients

Among patients with virological rebound and DRV FC In the DUET studies, adding ETR to a DRV/r containing regimen protects the activity of DRV/r in cases of virological rebound in HIV-1-infected, highly treatment-experienced patients with existing PI resistance at baseline

Here are links to 3 studies/articles on non-AIDS cancers and serious diseases and their death rates: the D.A.D. Study and the French Study report 2 weeks at the Lipodystrophy Workshop in London. Studies are finding that HIV viral load and CD4 count are associated with developing cancers and other comorbidities, so keeping a high CD4 count and undetectable viral load are crucial to preventing these comorobidities and cancers:

A quarter of drug trials submitted in support of new drug applications to the US Food and Drug Administration (FDA) remain unpublished five years after the fact, says new research published in the open access journal PLoS Medicine.

Among those trials published, unexplained discrepancies between the FDA submissions and their corresponding publications—the addition or deletion of outcomes, changes in the statistical significance of reported outcomes, and changes in overall trial conclusions—tended to lead to more favorable presentations of the drugs in the medical literature available to health care professionals.

Lisa Bero and colleagues from the University of California San Francisco reviewed the publication status of all 164 efficacy trials carried out in support of the 33 new drug applications (NDA) for new molecular entities approved by the FDA in 2001-2002, and compared information from the FDA reviews with published journal articles. Seventy-eight percent of the trials were published. Trials with favorable outcomes for the drugs were more likely to be published as those without favorable outcomes. Of a total of 179 primary outcomes included in the NDAs, 41 were omitted from the papers. The papers included 138 outcomes that were also in the NDAs (77%), plus 15 additional outcomes that favored the test drug, and two other neutral or unknown additional outcomes. Thus, the papers included more outcomes favoring the test drug than did the NDAs, report the authors.

The research also found additional discrepancies between the FDA reviews and the published papers. Of the 43 primary outcomes reported in the NDAs that showed no statistically significant benefit for the test drug, only half were included in the papers; for five of the reported primary outcomes, the statistical significance differed between the NDA and the paper and generally favored the test drug in the papers. Nine out of 99 conclusions differed between the NDAs and the papers; each time, the published conclusion favored the test drug. The authors did not investigate why the discrepancies existed, nor whether the changes were prompted by the drug sponsor, authors, or journals.

Because of their findings of publication bias and selective reporting, the authors conclude that "the information that is readily available in the scientific literature to health care professionals is incomplete and potentially biased."

In a commentary on the research, An-Wen Chan from the Mayo Clinic in Rochester (uninvolved in the study) says this new research makes an important contribution to the growing body of evidence that the trial literature is skewed towards reporting favorable results. "Biased reporting of results from NDA trials is particularly concerning because these journal articles are the only peer reviewed source of information on recently approved drugs for health care providers, who will have had limited clinical experience with these new treatments," Dr Chan says. "There are also substantial cost implications if the efficacy is overestimated and the drugs overused."

Before a new drug is approved for the treatment of a specific disease in the United States and becomes available for doctors to prescribe, the drug's sponsors must submit a "New Drug Application" (NDA) to the FDA, which provides details of the drug's development from laboratory and animal studies through to clinical trials. FDA reviewers use this evidence to decide whether to approve a drug.

Happy and astounding developments to be sure. How long, if this is as good as it appears to be, would it be before it can get to the masses? It clears the virus? That is what they're thinking? Then how long, how much parsing of the results would they need? Months? Years?

PS is a lipid molecule usually found on the inside of cell membranes that "flips" and becomes exposed on the outside of the membranes of virally infected cells and enveloped viruses. Exposed PS is known to be immunosuppressive and could potentially enable viruses to evade immune recognition. By masking the exposed PS, Peregrine's antibodies may block these immunosuppressive signals and allow the body to develop a robust immune response to the viral pathogen. Anti-PS antibodies have been shown to help clear infectious virus from the bloodstream and to induce antibody-dependent cellular cytotoxicity, an important anti-viral immune response. Researchers have found that PS is exposed on the outer membrane of cells infected with HIV, influenza, hemorrhagic fever viruses, CMV, herpes simplex viruses and smallpox viruses.

In addition to its potent anti-viral activity in lethal viral disease models, Peregrine's anti-PS antibody bavituximab appeared safe and well tolerated with promising signs of anti-viral activity in Phase I trials in patients with chronic HCV infection. Based on these positive data, Peregrine has initiated a trial in patients co-infected with HCV and HIV, a population that in the U.S. includes about 30% of all HIV patients.

As such, the anti-ps won't purge the latent reservoirs but work like the HAART.As it seems to have much less side effect, and as so far, no resistances issues is expected nor have been observed (with only few data), the anti-ps is a good news.

Now what I don't necessarly like with anti-ps is that it let the cells to be infected.So better would be to use it still with HAART. If so, what would be its added value ?I guess it's added value will come with the use of others immune therapies, and not HAART.

Now if the trials shows that using anti-ps alone is enough to become undetectable without having our immune system to overwork constantly to get this result, then it's a fantastic news.

Anti-ps will purge the infected reservoir cells because that same phosphlipid flip occurs on cd4 cell infected with the virus and in those cells hiding in reservoirs. The trick is to get enough antibodies in you system to teach your immune system to do the job on its own. See Could this be the Holy Grail? and read the patents. Exciting!

Selenium May Slow March Of AIDSIncreasing the production of naturally occurring proteins that contain selenium in human blood cells slows down multiplication of the AIDS virus, according to biochemists.

"We have found that increasing the expression of proteins that contain selenium negatively affects the replication of HIV," said K. Sandeep Prabhu, Penn State assistant professor of immunology and molecular toxicology. "Our results suggest a reduction in viral replication by at least 10-fold."

Selenium is a micronutrient that the body needs to maintain normal metabolism. Unlike other nutrients, which bind to certain proteins and modulate the protein's activity, selenium gets incorporated into proteins in the form of an amino acid called selenocysteine.

These proteins – selenoproteins – are especially important in reducing the stress caused by an infection, thereby slowing its spread.

Upon infecting a person, the virus quickly degrades selenoproteins so that it can replicate efficiently. It is unclear just how the virus is able to silence these proteins but Prabhu and his colleagues believe that stress inflicted on cells by the rapidly dividing virus, which produces a key protein known as Tat, is the likely culprit.

Tat is one of about 14 odd proteins produced by HIV during the first stage of infection. The job of these proteins is to trigger the expression of all the other genes that the virus needs to sustain itself. In addition, Tat also plays a key role in helping the virus replicate.

One of the proteins that targets Tat is a selenoprotein known as TR1.

"Since HIV targets the selenoproteins, we thought that the logical way to deal with the virus is to increase the expression of such proteins in the body," explained Prabhu, whose team's findings are outlined this week (Nov. 28) in the Journal of Biological Chemistry.

Researchers first isolated blood cells from healthy human volunteers who did not have HIV, and infected those cells with the virus. Next, they added tiny amounts of a selenium compound – sodium selenite – into the cell culture to see the effect on viral replication.

Results from the tests indicate that the addition of selenium inhibits the replication of HIV at least 10-fold, compared to cell cultures in which no selenium is added. When the researchers selectively reduced production of the selenium containing TR1 protein, they observed a 3.5-fold increase in viral replication.

"This confirms that while increasing the expression of TR1 has a negative impact on the replication of HIV, reducing it helps the virus replicate more efficiently," explained Prabhu. He believes that TR1 works by upsetting the chemical structure of Tat, which in turn reduces the virus' ability to replicate.

"Once we fully understand the function of these selenium proteins, it will give us a handle to come up with more effective drugs," said Prabhu, whose work is partly funded by the National Institutes of Health.

Phase I Clinical Trial To Test Combination Of Two HIV Vaccine Candidates Starts In LondonThe International AIDS Vaccine Initiative (IAVI) and the St. Stephen’s AIDS Trust at the Chelsea and Westminster Hospital have initiated a Phase I clinical trial in London, UK to test a prime-boost combination of two HIV vaccine candidates.

“Prevention is crucial in the fight against HIV and AIDS, and a vaccine is one of the most powerful prevention tools we know to combat infectious diseases,” said Professor Brian Gazzard, Research Director at the St. Stephen’s AIDS Trust and the principle investigator of this trial. “We hope this trial will contribute to a better understanding of how to induce with a vaccine an immune response to protect against HIV infection and AIDS.”

The news follows promising results recently announced by IAVI and partners for one of the two vaccine candidates to be tested, the MVA-based TBC-M4, which in a recent phase I trial generated modest immune responses in all volunteers who received the highest dose. According to Patricia Fast, Chief Medical Officer at the International AIDS Vaccine Initiative, “The responses observed with this vaccine candidate warrant further research to improve immune activation. We have learned from other studies that a prime-boost regimen has the potential to achieve just this.”

That is why the new trial will include a DNA-based vaccine candidate called ADVAX to prime the immune system. Previous Phase I studies with different DNA and MVA-based HIV vaccines in combination have shown that this prime-boost regimen was safe and well tolerated, and also able to generate enhanced immune responses when compared with the responses generated by either vaccine alone. The ADVAX vaccine candidate also offers economic value; it is relatively easy and cheap to manufacture, which makes it particularly appealing for use in the developing world.

A separate Phase I trial testing ADVAX and the MVA-based candidates in a prime-boost regime is planned for India. This trial would use a different mode of administration for the priming vaccine, different dosages and different vaccine regimens. Collectively, the results of both trials will help determine whether further development of both AIDS vaccine candidates in a prime-boost combination is warranted.

Deborah Jack, Chief Executive of the National AIDS Trust, comments: “The UK has always been a leader in the quest for new technologies to prevent HIV. Hosting a vaccine trial in London is a great opportunity to continue doing our part in the global fight against HIV and AIDS. Like any medical development, discovering an HIV vaccine is a naturally long process but when a vaccine is found it could save millions of lives globally, not just in the developing world but also in the UK.”

About the vaccine candidates

The vaccine candidate TBC-M4 is based on a vector built from recombinant Modified Vaccinia Ankara (MVA). It was designed by a biotech firm in the U.S. in collaboration with Dr. Sekhar Chakrabarty from the National Institute of Cholera and Enteric Diseases (NICED) in Kolkata, India . It targets HIV-1 subtype C, the most predominant HIV subtype in India, and contains 6 HIV genes : env, gag, reverse transcriptase, rev, tat and nef.

The vaccine candidate ADVAX is a plasmid DNA vaccine containing HIV-1 subtype C genes env, gag, pol, nef and tat. The vaccine was designed by the Aaron Diamond Research Centre in New York, through collaboration with Rockefeller University in New York and the International AIDS Vaccine Initiative.

It should be noted that since both vaccine candidates contain only synthetic copies of part of HIV’s genetic material, they cannot cause HIV infection.

ADVAX will be administered with a needle-free device (Biojector 2000), and the trial will also assess whether this delivery mechanism provides benefits over regular injection with a needle and syringe. ”Needle-free injection of a DNA vaccine can provide enhanced immune responses compared with administration by needle and syringe,” according to Dr. Richard Stout, Executive Vice President and Chief Medical Officer of Bioject Medical Technologies Inc., manufacturer of the device.

About the trial

The trial is a Phase I randomized, double-blind, placebo-controlled trial. It evaluates the safety and immunogenicity of ADVAX and TBC-M4 vaccines in a prime-boost regimen. The trial is recruiting 32 volunteers who are healthy HIV-negative men and women at low risk for HIV infection. All volunteers must provide full informed consent for their participation in the trial.

In addition to using standard immunology assays to measure the responses following vaccination, the trial will also evaluate a novel viral suppression assay. This assay provides a functional assessment of the immune response by measuring anti-viral activity. “There are indications from previous clinical studies that the laboratory assays currently used in HIV vaccine clinical trials are not an accurate predictor of whether a vaccine can prevent or control HIV infection,” said Dr. Jill Gilmour, Senior Director of Clinical Research at IAVI. “We urgently need to identify which laboratory tests give us insight into whether a person will resist infection with HIV or development of AIDS. This will enable researchers to select the most promising vaccine candidates for large-scale efficacy testing.”

It is expected that the trial will take 14 months to complete. The trial is fully sponsored by the International AIDS Vaccine Initiative.

Merck & Co has presented data on Gardasil which shows that the vaccine, which is approved for cervical cancer, is also effective in the prevention of human papillomavirus-related disease in young men.

Data from a Phase III trial in men aged 16 to 26, which was presented at the European Research Organisation on Genital Infection and Neoplasia meeting in Nice, France, showed that Gardasil prevented 90% of external genital lesions caused by human papillomavirus types 6, 11, 16 and 18. These are the only data evaluating efficacy of any HPV vaccine in preventing disease in males, Merck noted.

In the study, 4,065 males received three injections of either Gardasil or placebo over a six-month period. The results showed that after a mean duration of about 29 months, three cases of genital warts were observed in the Gardasil group, compared with 31 for placebo. The jab was also found to be 85.6% effective at reducing persistent HPV infection.

Merck said that is on track to submit a supplemental Biologics License Application for Gardasil to the US Food and Drug Administration by the end of the year. The vaccine is currently approved for use in females aged 9 to 26 to prevent cervical, vulvar and vaginal cancers caused by HPV strains 16 and 18, and genital warts caused by HPV types 6 and 11.

An approval for males would provide a huge boost to Gardasil sales which has fallen off recently after its extremely successful launch in 2006. Third-quarter revenues from the vaccine were down 4% to $401 million.

A new clinical trial to test the effectiveness of pre-exposure prophylaxis in stable sexual relationships has started in Uganda, with 3,900 discordant couples enrolled in a five-year study.

"The aim of the study is to find out whether pre-exposure prophylaxis [PrEP] prevents HIV acquisition within HIV discordant couples," said Dr Jonathan Wangisi, principal investigator of the study.

The AIDS Support Organisation (TASO), the Institute of Infectious Diseases (IDI) and the US Centres for Disease Control (CDC) will conduct the study in various districts of Uganda. The trials are being undertaken in partnership with the University of Washington, Seattle, and the Bill and Melinda Gates Foundation.

If successful, the project will present a new HIV-prevention method that focuses on a non-traditional high-risk group that has not adequately been targeted. According to the government, at least 42 percent of all new infections in Uganda occur in stable sexual relationships.

The study could also make PrEP a major tool in the fight against HIV/AIDS, and present discordant couples - where one partner is HIV-positive and the other negative - with a means to have children without fear of infecting the HIV-negative partner.

Wangisi said a pill with either tenofovir, or a combination of tenofovir and truvada - both highly effective life-prolonging antiretroviral (ARV) drugs - or a placebo, would be given to the HIV-negative partner. The pill is to be taken orally every day at a time agreed among the participants in the different study sites.

Several recent studies have shown that the odds of the negative partner in a discordant heterosexual relationship becoming infected are very low when the positive person's viral load has dropped significantly as a result of treatment.

The study has a high risk of transmission, so all participating discordant couples will be counselled and encouraged to use all available HIV-prevention measures, including male circumcision, abstinence and condoms.

"PrEP is not a substitute for condoms or other proven HIV-prevention strategies, it is an addition," Wangisi said. "Condoms, if used regularly and properly, are the best medical intervention in HIV prevention for those that cannot abstain."

Dr Kihumuro Apuuli, director-general of the Uganda AIDS Commission, said the study was necessary because of the reported low condom use among HIV-discordant couples and few people knew the HIV status of their long-term sexual partners.

Only 21 percent of Uganda's 30 million people have ever been tested for HIV, but estimates have put the number of new infections at over 100,000 annually, and at least 1.1 million people are infected with HIV.

Powerful drugs to treat HIV mean it no longer is a death sentence. But longer life means fighting the same illnesses that people without HIV face, including diabetes and high blood pressure.

For HIV-positive diabetics suffering from kidney failure, the possibility of a transplant was uncertain.

Antirejection drugs could further weaken infected immune systems, possibly leading to infections and complications.

"Everybody was afraid to give HIV-positive people ... heavy drugs to prevent rejection," said Scott Gruber, a Wayne State University transplant surgeon at Harper University-Hutzel Women's Hospital in Detroit.

But between 2004 and 2008, Gruber gave nine HIV-positive patients on a general transplant list new, HIV-negative kidneys. So far, eight have been successful.

"They have to be monitored closely, but HIV should not be considered an automatic" exclusion "for a kidney transplant," he said.

Fueling drug development is an ever-changing set of HIV proteins that make the virus drug-resistant.

Ladislau Kovari, a biochemist at WSU, studies crystals of an HIV enzyme called protease.

Comparing the structure of the normal enzyme to a drug-resistant variety allows him to design better drugs to treat the 10% to 25% of people who may have drug-resistant HIV.

Frenchmen fancied themselves to be the most sexually endowed in a study of European men who were asked to measure their penis.

The survey of more than 10,500 men in 25 European countries was conducted by the German-based Institute of Condom Consultancy, The Daily Telegraph reported Saturday.

Frenchmen topped the survey, claiming an average penis length of 6.09 inches [15.46 cm] -- 1.2 inches [3 cm] longer than Greeks, who had the shortest average among men participating in the survey, the Telegraph reported.

At its annual fair -- called "Pimp Your Condom" -- the Institute gives advice on condom size and how to avoid sexually transmitted diseases, said Jan Vinzenz Krause, the institute's director, who once proposed an aerosol latex spray-on condom in a can.

Two locally developed test HIV vaccines are nearing phase I clinical trials in humans. The vaccines, developed by research teams led by the University of Cape Town will be tested in both South Africa and the USA.

The test vaccines – called SAAVI MVA-C and SAAVI DNA-C2 – have undergone laboratory and animal testing, and will now enter phase 1 human clinical trials. The DNA vaccine was wholly developed by South Africans - a team of scientists at the University of Cape Town’s Institute for Infectious Diseases and Molecular Medicine and manufactured by Althea Technologies in the USA. The MVA vaccine was conceptualised by the team at the University of Cape Town and developed and manufactured with input from international biotech company, Therion, and the United States National Institutes of Health (NIH). The vaccines have been in development since 2002 and the project has been funded by the South African AIDS Vaccine Initiative and the NIH. Both vaccines were manufactured in the USA. The vaccines are specifically targeted at the HIV-1 strain C that accounts for the majority of infections in southern Africa.

The trial is a phase I trial involving 36 people at two sites in South Africa – one in Cape Town and one in Johannesburg and 12 people in the USA.

The trial has already been approved by the United States Food and Drug Administration and by the Medicines Control Council in South Africa. This phase I trial is scheduled to start in Boston in the first week in December 2008, in the USA . Testing in South Africa will start in early January 2009.

A phase I trial for an HIV vaccine generally involves volunteers who are at low risk for infection, who do not engage in risky sexual behaviours or intravenous drug use. A phase I trial primarily tests for safety, tolerability and side effects but also starts to look at the effect of the vaccine on the human immune system. If successful, a phase I trial is followed by larger phase II and III trials which involve more volunteers and provide information on whether the product is able to protect against infection. A vaccine can only be licenced for public use after it has been tested and found successful in all three phases.

South Africa has been involved in a number of clinical trials for HIV test vaccines since 2003 but this will be the first for products developed in South Africa by South African scientists.

SAAVI is extremely gratified that these test HIV vaccines are entering human clinical trials. However, there is still a long way to go before we will know if these products will be in any way successful in preventing HIV infection.

The genome of a squirrel-sized, saucer-eyed lemur from Madagascar may help scientists understand how HIV-like viruses coevolved with primates, according to new research from the Stanford University School of Medicine. The discovery, to be published online on Dec. 1 in the Proceedings of the National Academy of Sciences, could provide insight into why non-human primates don't get AIDS and lead to treatments for humans.

Scientists have long believed that lentiviruses — the family of viruses that includes HIV — started infecting primates within the past million years. In fact, said Rob Gifford, PhD, former postdoctoral researcher in infectious diseases and geographical medicine and lead author of the new study, lentiviruses may have been present in ancestral primates as long as 85 million years ago.

A type of retrovirus, lentiviruses replicate by inserting their RNA into a cell's DNA. Some retroviruses have been known to infect cells that mature into sperm or eggs, incorporating viral DNA into the genome of the host. Until last year, when Gifford discovered Rabbit Endogenous Lentivirus type K among the DNA of the European rabbit, no one knew lentiviruses could be inherited in this way.

"It allows us to put a timeline on the evolution of primate lentiviruses," said Robert Shafer, MD, associate professor (research) of infectious diseases and geographical medicine and senior author of the paper.

Gifford began computer-based screening of the DNA of 21 primates for which at least partial genome sequencing was available. He searched each species for strings of nucleotides that matched the modern lentivirus genome and found one lurking in the DNA of the tiny gray mouse lemur.

Ancestors of the modern lemur colonized Madagascar about 75 million years ago, and since then, lemurs and their lentivirus-carrying African cousins have been evolving separately. Four hundred kilometers of ocean divide the two branches, giving mainland primates limited opportunities to swap germs with lemurs. And the last of the occasional land bridges between the two disappeared beneath the sea 14 million years ago, suggesting that lentiviruses are likely at least that old, say the researchers.

High-end estimates of the age of this lentivirus, called pSIVgml, could range back 85 million years, when the primate family that includes lemurs split from the evolutionary branch that would eventually give rise to monkeys, apes and humans. "Lentiviruses could be very ancient indeed," Gifford said.

Gifford remains cautious about overestimating the virus's age, warning that the virus could have been spread within the last 14 million years by something that could cross the ocean, such as a bat. But Shafer says that sort of cross-species transmission is unlikely, because bats and primates are very distant relatives. The leap from primate to bat and back would be difficult for a lentivirus to make.

Gifford's find suggests lentiviruses could be discovered in other places they've never been seen, like Asian and New World monkeys. "As far as we're aware, nobody's really looked that hard," said Gifford. He is one of few researchers using genome databases to search for retroviruses.

Finding widespread lentivirus-primate interaction might open doors for HIV/AIDS research. Primates infected with the simian version of HIV are protected from developing AIDS by several genes which code for proteins in the immune system that slow or block retroviral reproduction. Previous research suggests these genes evolved in response to millions of years of retrovirus infection.

Until now, scientists thought lentiviruses were too young to have participated in this evolutionary back-and-forth. But if Gifford and his colleagues find more evidence that lentiviruses and primates have been in each other's genetic business for many millions of years, they could turn that assumption on its head. In the process, they might lead the way to a deeper understanding of the evolution of ancient innate immune defenses against retroviruses, which could have implications for HIV treatments or vaccines.

The research "raises a bunch of interesting questions about how mammals have dealt with these types of viruses over a minimum of 14 million years, what kind of defenses they have developed, and why some mammal species have lost these type of viruses," said Beatrice Hahn, PhD, a professor in the department of medicine at the University of Alabama at Birmingham who studies human retroviruses. She hopes to see more research into the presence of lentiviruses in mammal genomes. "This is molecular archaeology," she said. "There may be a lot of gold in these sequences that hasn't been mined yet."

Gifford and Shafer collaborated on this study with researchers from the Imperial College of London and the Institute for Emergent Infections at the James Martin 21st Century School at Oxford. The research was supported by the National Institute of Allergy and Infectious Diseases and the James Martin 21st Century School.

Obama promises to leave behind ideology-driven debates over how to spend money, and instead put common sense and science first.

Like so many millions of Americans, on November 4 I sat with friends and watched in awe as America elected Barack Obama to be our 44th president. And for the past two weeks, I've been trying to understand what all this means, especially for people with HIV in the US and worldwide. In this time of transition, I've realized it's helpful to look back on where we've been in order to get an idea of just how historic this election is.

So, let's go back in time, to May of 2007. President Bush has just given a speech outlining his vision for the next five years of U.S. global AIDS efforts. In short, he said "we should keep doing what we're doing, not learn any lessons, keep pushing abstinence, and flat fund the program." This was on top of six and half years of wholesale neglect of the domestic AIDS crisis. In response, activists got together and developed a platform that laid out exactly what the next president would need to do to undo the harm of the Bush administration's AIDS plan, while continuing the parts that are doing good and saving lives.

We set out on a mission -- to convince each of the candidates for office that they needed to support our plan, which included such novel ideas as promoting comprehensive sex education, advancing generic drug access and spending $50 billion over five years on AIDS around the world. While we made some progress, the fight against AIDS was overshadowed by other issues shaping the campaigns, such as the war, healthcare and the economy.

Then, a little over a year ago, several hundred people marched through the streets of Philadelphia to the doors of the Democratic debate, and demanded AIDS plans from each of the Democratic candidates for president. Shortly after, all eight candidates had released comprehensive plans to fight AIDS, including our current President-elect and Vice-President-elect. Their plans were modeled in large part on a platform many of us had been advocating for months.

Taking a look at Obama's AIDS plan (PDF) is like reading my policy wish list. He promises to leave behind ideology-driven debates over how to spend money, and instead put common sense and science first. He wants to end our funding of programs that only discuss abstinence and fidelity without a mention of condoms. He would no longer negotiate harmful trade deals that prioritize drug company profits over people's lives. And he wants to invest fully in the fight against global AIDS, both through bilateral programs and the multilateral Global Fund to Fight AIDS, TB, and Malaria.

Domestically, his plan is spot-on. He's calling for the development of a National AIDS Strategy, including expanding Medicaid to cover people with HIV, not just AIDS, and ending the federal ban on funding for syringe exchange. He recognizes that we must do more to confront the epidemic of HIV communities of color, especially amongst gay men and other men who have sex with men, and calls for action on this issue.

Unlike Bush's plan detailed in May of 2007, we won a plan from Obama that uses many of the real tools we have to fight the epidemic. In two months and two days, President Obama will become the 44th president of the United States. We have much to be hopeful for, but we also know that he is going to face incredible challenges to enact his visionary plan. In the midst of a financial crisis, programs aimed at the poorest people are easy to push aside for a few months or a few years. We need to let President-elect Obama know we support him, and we support him implementing his AIDS plan.

In two days, one thousand activists will do just this. People living with HIV, and allies, from across the country are coming to DC to rally behind Obama's AIDS plan, and call for him to take steps to implement it in his first 100 days in office. We'll be holding an "inauguration ceremony and parade," and will march to the White House and transition team offices.

The AIDS crisis, both domestically and globally, is not something that can be ignored any longer. No president has ever taken fighting AIDS, especially at home, seriously. We're on the verge of inaugurating the first person that not only can help us end the AIDS epidemic, but has the plan to do it, too. We're hopeful that he will really do what he says he's going to do. But we're also taking action, and rallying behind his plan, because we know that grassroots action is the only way we'll really end the AIDS epidemic.

HIV proteins and cellular controlThere are a multitude of potential targets that researchers throughout the world are studying in the fight against HIV, but this virus seems to have an answer for most of them.

HIV is an extraordinarily smart virus. Just as researchers track down another potential vehicle for halting its spread, it throws up another roadblock. Research on vaccines has been ongoing for 20 years, with neutralising antibodies remaining the best hope after the recent failure of Merck’s Phase III trial of an adeno-vectored T-cell vaccine, but at the moment combination antiretroviral therapy is our only weapon.

As HIV has a relatively limited number of its own proteins, researchers have obviously zeroed in on these to try to inhibit viral replication. The virus’s ability to mutate has sidestepped many of these attempts, however, so some are looking at inducing the cellular mechanism known as RNA interference to halt the virus in its tracks by silencing gene expression. Even then, however, HIV might have a solution.

Associate Professor Damian Purcell, who heads the Molecular Virology Laboratory at the University of Melbourne, has been experimenting with RNAi since he first heard that it functioned in mammals at the 2001 RNA Society conference addressed by Tom Tuschl, one of the discoverers of mammalian microRNAs (miRNA) who also found that RNAi functions in mammalian species.

Like many, Purcell rushed back to his own laboratory and began designing short interfering RNAs (siRNA) – the small strands of RNA that bind to complementary sequences of messenger RNAs and silence gene expression post-transcriptionally – as a way of targeting HIV. However, as everyone else discovered, HIV is often able to rapidly escape control by siRNAs, its mutability working in its favour yet again.

That doesn’t mean RNAi may not prove a potent weapon against HIV, as the multitude of clinical studies currently underway illustrate. It’s just that many viruses, especially HIV, have evolved with the ability to counter these cellular control mechanisms, so designing the right siRNA is paramount. short hairpin RNAs (shRNAs) are also in development. For example, in October a trial of an shRNA-based RNAi therapy in HIV patients released promising – although very early – results.

Silencing HIV genes using siRNAs and shRNAs does reduce viral replication and as such is a very promising line of enquiry. Like many others, Purcell’s laboratory has designed lentivectors for delivery of siRNA to target HIV, but his team has also pursued other protein targets, in particular cellular proteins that do not mutate and therefore may provide an alternative route.

One target is the HIV trans-activation response RNA binding protein (TRBP), which inhibits the RNA-dependent protein kinase (PKR) response. TRBP binds to PKR, one of the main interferon-response proteins that shut down the expression of viruses in cells, and in HIV infection keeps the PKR pathway from doing its job.

Purcell’s lab has been studying TRBP for many years and has uncovered some surprising activities of the protein in astrocytes. The researchers have also discovered that TRBP turns out to be an essential component of the miRNA biogenesis pathway – it is a binding partner for Dicer, the protein that cleaves double-stranded RNA into siRNAs and sets off the whole RNAi cascade.

“It has been an interesting observation – almost a roadblock – that the TRBP molecule turned out to be an essential component of the RNAi pathway,” Purcell says. “It turns out that it’s a very good target (for inhibition) but that also eliminates the ability to produce siRNAs.

“There’s a lot that we don’t understand in the control of gene expression at a post-transcriptional level and viruses are very busy in this area. Many of them make proteins that are able to defend against these cellular control mechanisms, and curiously the same viral proteins that inhibit PKR also inhibit RNA interference.”

Astrocytes and innate immunity

Our understanding of these viral proteins, and how our own immune system is unable to counteract them, has been much improved by studying astrocytes, the glial cells that for some reason do have a natural resistance to productive HIV infection. In 2005, Purcell and colleagues from the University of Melbourne and from McGill University in Canada looked at how astrocytes manage to silence HIV infection.

No one really knows exactly how it is done, but while astrocytes are infected by HIV, the virus’s RNA is unable to produce proteins in these particular cells. “Astrocytes are naturally infected but curiously the infection goes through all of the steps of entry and integration of the virus, and it even transcribes large amounts of RNA, but those RNAs don’t seem to yield proteins,” Purcell says. “It is blocked at a post-transcriptional level and we thought that was interesting.

“One of the things that seemed to be a candidate at the time was the known interferon response pathways involving PKR. We suspected that TRBP was a binding partner and a cellular control protein for the level of responsiveness for the PKR pathway.”

“When we supplied (TRBP) back to those cells at higher levels we could restore efficient HIV production. We don’t know exactly the reason but we suspect that in the brain a lot of these genetic pathways for antiviral responses have to be more sensitive than elsewhere as you can’t afford to have an expanding T cell response in the brain, for example.”

With the discovery that TRBP is a binding molecule for Dicer, and his work on the remarkable ability of astrocytes to fend off HIV by keeping TRBP at low levels, come some fascinating research potentials. “What the research is finding now is a convergence between this innate immune pathway involving PKR and interferon, which we’ve known about for a long time, and how through TRBP this connects to the genetic immune system of RNA interference. What we’ve been trying to figure out is the relative importance of RNAi compared with the PKR-interferon-driven pathway in the control of HIV.”

In addition to looking at some of the cellular proteins, Purcell and his team are of course looking at HIV’s small but powerful complement of viral proteins, as well as the RNA elements that make HIV such a fascinating and challenging virus to study.

Tat Rev, Nef and Vif are intensely studied around the world, as is the envelope, or Env, protein, which is of great interest in vaccine development. “Over the years we have been interested in understanding what virus RNA elements we must retain in order to preserve optimum expression of the viral proteins for our various HIV vaccines, without keeping so much that we allow them to reconstitute an infectious pathogenic agent,” he says.

“We’ve looked at the functions of the small control proteins Rev and Tat, but in recent times our vaccine efforts have focused on envelope, because we are very keen on understanding how we can express many different envelopes and assess them as candidate vaccines for neutralising antibodies, because that seems to be the best hope for an effective HIV vaccine.”

With the limited resources that all Australian researchers must face, Purcell has decided to take a different angle in potential vaccine development – the understanding of how the different RNA elements work to control efficient envelope expression in HIV.

Purcell says that one of the most fascinating aspects of using HIV as a model genetic system is that it must obey the rules of human genetics to survive. “Many of the things that have been observed with post-transcriptional control mechanisms have turned out to also operate in certain cellular genes during later analysis. HIV is a fairly plastic genetic system and is easy to study and manipulate, and has revealed many new mechanisms.”

Functional RNAs

Associate Professor Damian Purcell started out in molecular immunology at a time when virology wasn’t exactly booming in Australia. He did his PhD in the early 80s with Ian McKenzie, the former head of the Austin Research Institute, looking at the genetics of cancer and then moving on to endogenous retroviruses.

“Then HIV appeared, right when I was a starting PhD student,” he says. Purcell was working on gibbon ape leukaemia virus and making antibodies against what he thought might be a new human virus, and was collaborating with the now famous Robert Gallo lab at the University of Maryland.

“He was working on these kinds of viruses and I went over to one of the early Keystone conferences in 1985, when they’d just finished their work identifying the HIV virus,” Purcell says. “I wanted to talk to him about what we thought was a human endogenous retrovirus, but he said ‘thank you, but we’re frankly just not interested because HIV is so important. We’ve dropped all that other stuff and we’re just working on HIV.’ He was right.”

Purcell then received a CJ Martin Fellowship and went to the US National Institutes of Health to work with Malcolm Martin, who did a lot of the early molecular biology of HIV. “In that lab they were very interested in RNA elements and the functions of small RNAs, so I’ve been interested in functional RNA since then.”

Intradigm Corporation has announced the issuance of United States patent 7,459,547, entitled "Methods and Compositions for Controlling Efficacy of RNA Silencing."

The issued patent, which is based on the seminal research of Philip Zamore, Ph.D., the Gretchen Stone Cook Chair of Biomedical Sciences and Professor of Biochemistry & Molecular Pharmacology at University of Massachusetts Medical School, generally claims methods of enhancing the RNA silencing activity of an RNAi agent through certain structural modifications in various cell types, including mammalian. The issued claims not only focus on siRNA but also include specific claims directed to micro RNA (miRNA), pre-miRNA, and short hairpin RNA (shRNA). This patent issues from a portfolio of several applications disclosing efficacy-enhancing methods and structural elements of RNAi therapeutics that Intradigm has exclusively licensed from the University of Massachusetts Medical School.

"There is little dispute among those involved in the RNAi sector that proper siRNA structure and design is taking on an increasingly important role in the development of next generation RNAi therapeutics," said James Topper, M.D., Ph.D., general partner at Frazier Healthcare Ventures and chairman of Intradigm's board of directors. "Accordingly, the siRNA structure claims of this issued patent provide Intradigm with another important tool in the company's efforts to realize the tremendous therapeutic promise of RNA interference."

"Ongoing scientific research has highlighted the importance of siRNA structure as a critical component of an effective RNAi therapeutic and the issuance of this patent provides Intradigm with a significant competitive advantage in this area," said Mike Riley, Intradigm's vice president of intellectual property and corporate development. "For Intradigm, this patent becomes even more valuable when combined with the company's proprietary RNAi sequences and delivery technologies. Ultimately, access to this intellectual property will allow Intradigm to create a high value pipeline of well- protected products developed by incorporating novel, enhanced RNAi sequences into the company's innovative RNAi delivery systems."

Intradigm possesses one of the industry's strongest RNAi IP positions including key assets strategically licensed from both the University of Massachusetts Medical School and the Massachusetts Institute of Technology (MIT). The company's IP estate of issued patents and pending applications broadly covers structural features for a next generation of RNAi molecules, biodegradable polycationic polymers for the delivery of RNAi therapeutics, and proprietary siRNA sequence applications.

Gilead Sciences Inc. (GILD: News ) said the results of two late-stage trials showed that its Viread is significantly more effective in treating the virus that causes chronic hepatitis B than Hepsera, which is also developed and marketed by Gilead.

Data also indicate that at week 48, Viread was superior to Hepsera in reducing HBV DNA levels to below 400 copies/mL and was comparable to Hepsera in achieving histological response, the company noted.

Next Generation RNAi Technology Discovered by AiRNA Pharmaceuticals and Boston BiomedicalAiRNA Pharmaceuticals, Inc., a RNAi therapeutics company based on next generation proprietary RNAi technologies, and Boston Biomedical, Inc., a biotechnology company developing novel therapies targeting cancer stem cells, today announced that asymmetrical interfering RNA (aiRNA), a new fundamental RNAi technology discovered by the companies, is being published in the December issue of Nature Biotechnology. The publication titled "Asymmetric RNA Duplexes Mediate RNA Interference in Mammalian Cells" highlights that the smaller 15 bp aiRNA can target a variety of genes with superior efficiency than the standard 19-21 bp siRNA. Furthermore, the new aiRNA structure can target genes more selectively with significantly less off-target effects than the standard 19-21 bp siRNA. These results establish aiRNA as a new and superior structure to silence genes.

"We are extremely excited by the discovery of the aiRNA technology given its broad and profound potential for medicine and its superior gene silencing properties" said Dr. Chiang J. Li, senior author of the article, Chairman and Chief Executive Officer of Boston Biomedical. "We believe this break-through will have far reaching benefits in the development of RNAi therapeutics, particularly with the technology's potential ability to target any of the disease-causing genes."

The new aiRNA technology centers on proprietary asymmetric structures which contrasts with the current paradigm that relies primarily on symmetric siRNA duplexes of 19-21 bp in length. The novel asymmetric structure is responsible for the gene silencing advantages of aiRNA, including reduced off-target effects, improved gene silencing efficiency, durability, and reduced synthesis cost.

The discovery of RNAi promises to revolutionize medicine due to its unlimited potential to treat genetic, epigenetic and infectious diseases. The siRNA-based approaches have met with many challenges including non-specific off-target effects, synthesis cost, and limited efficacy for some genes. The new aiRNA technology may help to unleash the enormous potential of RNAi as a whole new class of therapeutics for human diseases.

RNAi (RNA interference) is a revolutionary discovery in biology with broad and profound implications for biology and medicine, and was awarded the 2006 Nobel Prize for Physiology/Medicine. RNAi is a natural cellular process and a catalytic mechanism of gene silencing. The discovery of RNAi promises to revolutionize medicine due to its unlimited potential to treat genetic, epigenetic, and infectious diseases. Such a natural process can, in theory, be harnessed to target any disease genes, including "undruggable" targets. Like antibody technology, RNAi may have the enormous potential to become an entirely new class of drugs for human medicine.

NEW YORK, Nov 25, 2008 ----The U.S. Food and Drug Administration (FDA) has granted SELZENTRY(TM) (maraviroc) full (traditional) approval for use in treatment-experienced adults with CCR5-tropic HIV-1 in combination with other antiretrovirals. SELZENTRY was originally granted accelerated conditional approval in August 2007 based on 24-week data from pivotal Phase 3 studies. SELZENTRY now becomes the latest fully approved treatment for HIV.

"New, effective and well-tolerated treatment options are critical for treatment-experienced persons living with HIV infection," said W. David Hardy, MD, Chief of the Division of Infectious Diseases, Cedars-Sinai Medical Center and Associate Professor of Medicine at the David Geffen School of Medicine, University of California, Los Angeles (UCLA). "Selzentry, the first oral entry inhibitor, has proven to be an effective and well-tolerated treatment option for treatment-experienced patients whose HIV has become resistant to other treatments, but remains susceptible to this new class of medications."

The full approval of SELZENTRY is based on 48-week data from the MOTIVATE (Maraviroc Plus Optimized Therapy in Viremic Antiretrovial Treatment Experienced Patients) studies. The studies compared the safety and effectiveness of SELZENTRY plus optimized background therapy to placebo plus optimized background therapy in treatment-experienced CCR5-tropic HIV-1 patients.

Accelerated conditional approval is granted to medicines that provide a meaningful therapeutic advantage over existing treatments for serious or life-threatening diseases. FDA grants full approval status once it is satisfied with longer-term safety and efficacy data. Once full approval is granted, restrictions on promotion and/or distribution that apply to conditionally approved medicines are removed.

"SELZENTRY has been on a long journey, from its initial discovery by Pfizer scientists in 2000 to this full FDA approval," said Dr. Howard Mayer, Pfizer's executive director, and development team leader for HIV/AIDS. "We are extremely excited with this important milestone in SELZENTRY's lifecycle and the potential improvement it may bring to treatment-experienced people living with HIV/AIDS."

Results at Week 48 from the MOTIVATE studies were recently published in the October 2, 2008 edition of the New England Journal of Medicine.

About SELZENTRY

SELZENTRY is part of a new class of drugs called CCR5 antagonists, providing a new approach to HIV treatment. A diagnostic test confirms whether a patient is infected with CCR5-tropic HIV-1, which is also known as "R5 virus". SELZENTRY blocks viral entry into CD4 T-cells that express the CCR5 co-receptor, stopping the R5 virus on the outside surface of the cells before it enters, rather than fighting the virus inside the cell, as do all other classes of oral HIV medicines.

Data Supporting SELZENTRY Full Approval

The full approval is based on 48-week data which showed that a greater log reduction in viral load from baseline was seen in patients receiving SELZENTRY plus optimized background therapy, compared to those patients receiving placebo plus optimized background therapy (MOTIVATE 1 and 2 pooled data = -1.68 log(10) copies and -1.84 log(10) copies/mL for SELZENTRY once-daily and twice-daily, respectively, compared with -0.79 log(10) copies/mL for placebo).

Results analyzed at 48-weeks showed no clinically relevant differences in the safety profile between the study treatment groups and remained consistent with 24-week results. The most common adverse events included upper respiratory tract infections, cough, pyrexia, rash, and dizziness.

Expect vaccine to inhibit HIV within 5 years: Nobel winnerA therapeutic vaccine to inhibit the spread of HIV will be available within five years, according to a Nobel Prize-winning scientist who helped discover the virus.

Luc Montagnier, director of the World Foundation for AIDS Research and Prevention, said he thinks it is "a matter of four to five years" before such a vaccine is developed. Restricting the transmission of HIV, he said, would change how the disease is managed and controlled.

Montagnier, 76, said a therapeutic vaccine, to be given to those who are already infected in order to inhibit the likelihood of transmission, would be a key step in fighting the virus. By comparison, a preventative vaccine would protect people from contracting HIV in the first place.

"Our job, of course, is to find complementary treatment to eradicate the infection. I think it's not impossible to do it within a few years," Montagnier said in Stockholm, according to Reuters.

"So I hope to see in my lifetime the eradication of, not the AIDS epidemic, but at least the infection. This could be achieved."

The French scientist did not explain why he believes the discovery will be made in that specific time frame. While medications exist that lessen the effects of the disease for those who have been infected, none has been created that prevents or cures an HIV infection.

About 33 million people across the world have been infected with the human immunodeficiency virus, or HIV.

Montagnier, along with his colleague Françoise Barré -Sinoussi, 61, won the Nobel Prize for medicine this year for their discovery of the virus.

Last May marked the 25th anniversary of the a report, published in the journal Science of by Montagnier and colleagues of La Pitie-Salpetriere Hospital and the Institute Pasteur in Paris that indicated they had discovered the cause of the then little-known disease known as AIDS.

"A retrovirus belonging to the family of recently discovered human T-cell leukemia viruses (HTLV), but clearly distinct from each previous isolate, has been isolated from a Caucasian patient with signs and symptoms that often precede the acquired immune deficiency syndrome (AIDS)," their report began.

Montagnier and his colleagues named the newly discovered pathogen lymphadenopathy-associated virus or LAV. But it was subsequently renamed the human immunodeficiency virus or HIV.

Barré -Sinoussi, who was also in Stockholm Saturday in advance of Nobel festivities that end with a banquet and awards ceremony Dec. 10, said scientists have a responsibility to try to use their work to inform public — and political — opinion.

"Still, 25 years after the HIV discovery, [there is] discrimination, stigmatization against HIV-infected individuals — even criminalization. This is not acceptable. This is really not acceptable," Barre-Sinoussi said, according to Reuters.

Residents of Islington Benefit from Free HIV Testing and CounsellingScores of residents from the community of Islington in St. Mary, benefitted from free HIV testing and counselling, at a health fair, organised by the St. Mary Health Department.

The event, held recently at the Islington Community Centre, was part of activities to mark World AIDS Day. HIV positive persons were sensitised about the importance of following the medical advice they received and adhering to the treatment prescribed.

Among other services provided were blood sugar and blood pressure tests, and counselling to parents and children, to encourage more effective parenting in the society.

Among the organisations providing services on the day were the Child Development Agency, the HIV Prevention and Control Programme, the Rural Agricultural Development Authority (RADA) and LIME.

Behaviour Change and Communications Officer for the St. Mary Health Department, Omar Marston, said he was satisfied with the day's activities, noting that the objectives of increasing awareness about HIV/AIDS, and providing general health care and advice to the people of the Islington community, were achieved.

He said he was pleased at the number of residents who requested HIV tests, noting that the results were made available on the same day.

According to Mr. Marston, the St. Mary Health Department feels a sense of satisfaction in being able to serve the parish and he urged residents to co-operate with the Department to ensure good health standards in St. Mary.

HIV infections among women in Malaysia are on the rise and more housewives than sex workers have been found to contract AIDS, according to a new report that has health planners worried.

With an average of 12 Malaysians testing positive for HIV daily, Malaysia has one of the fastest growing AIDS epidemics in the East Asia and Pacific region. What is more worrying is that the trend is gaining a feminine face, mainly through heterosexual transmission.

A new report released Thursday by the Malaysian Health Ministry and United Nations Children's Fund (Unicef) has revealed that the trend of new HIV infections amongst women rose drastically to 16 percent in 2007 from 1.2 percent of total new cases in 1990.

"The proportion of women reported with HIV has increased dramatically in the last decade. In 1990, only one in every 86 new HIV infections was amongst women and girls. As of December 2007, it was one in six new infections," Sultanah Bahiyah Foundation chairperson Safinaz said at the launch of the "Women and Girls Confronting HIV and AIDS in Malaysia 2008" report.

"Shockingly, surveys show that in 2006 more housewives tested HIV positive than sex workers," Safinaz said, adding that there are thousands of children living in homes shadowed by HIV.

She said for families affected by HIV and AIDS, the disease itself does not have so much impact as it can be kept under control for many years with effective treatment, The Sun newspaper reported.

"The biggest impact comes from stigma. Mothers whose families are affected by HIV and AIDS are most frightened by the reactions from friends, extended family, colleagues and their communities," she said, citing the case of a shopkeeper in Kedah who refused to allow a woman with HIV to enter his shop.

Unicef representative in Malaysia Youssouf Oomar said empowering and encouraging women to be leaders in any HIV response must be the strategy of the future.

"Malaysia must ensure that gender equality and empowerment of women go hand-in-hand with HIV and AIDS prevention and care programmes," he was quoted as saying by the newspaper.

A therapeutic vaccine to inhibit the spread of HIV will be available within five years, according to a Nobel Prize-winning scientist who helped discover the virus.Luc Montagnier, director of the World Foundation for AIDS Research and Prevention, said he thinks it is "a matter of four to five years" before such a vaccine is developed.[...]"Our job, of course, is to find complementary treatment to eradicate the infection. I think it's not impossible to do it within a few years," Montagnier said in Stockholm, according to Reuters.[...]The French scientist did not explain why he believes the discovery will be made in that specific time frame.

I'm curious to know whether this clown dared to tell the same vague old bullshit in his Nobel Lecture. Let's wait some days...

New Delhi, Dec. 7: Justifying criminalisation of homosexuality in the country, the Centre has pleaded before the Delhi High that it is one of the main reasons for spread of HIV/AIDS and needs to be curbed.In a written submission filed by additional solicitor general Mr PP Malhotra, the Centre said that legalising men having sex with men (MSM), as pleaded by gay rights activists, would lead to spread of the dreaded disease and placed reports of various countries to substantiate its stand.

Inflammatory blood vessel activation is enhanced in HIV positive people independent of antiretroviral therapy and lipoatrophy

Research increasingly suggests that inflammation associated with HIV infection contributes to the spectrum of non-opportunistic conditions -- including cardiovascular disease -- seen in HIV positive patients.

Research increasingly suggests that inflammation associated with HIV infection contributes to the spectrum of non-opportunistic conditions -- including cardiovascular disease -- seen in HIV positive patients, but the complex interactions between the virus itself, immune and metabolic changes, and antiretroviral therapy remain poorly understood.

But another study, published in the December 2008 Journal of Acquired Immune Deficiency Syndromes , indicates that inflammatory changes and endothelial activation affecting blood vessels occurs in HIV positive individuals who are not on ART and do not have lipoatrophy -- and that anti-HIV therapy may, in fact, reduce inflammation.

Allison Ross and colleagues assessed the association between inflammatory and endothelial activation biomarkers and the presence of lipoatrophy in HIV-infected patients. They also examined the roles of HIV itself, antiretroviral therapy, and metabolic parameters in endothelial activation and inflammation.

The prospective cross-sectional study included 182 participants seen at Case Western Reserve University in Cleveland, Ohio, divided into 4 groups:

• Strong correlations were observed between some inflammatory cytokines and endothelial markers.

Based on these findings, the investigators concluded that ART-naive HIV positive patients have enhanced endothelial activation, while HIV positive individuals on ART have values similar to those of healthy controls; furthermore, lipoatrophy did not seem to affect endothelial activation.

"In our study, we found no correlation between limb fat and any endothelial or cardiovascular marker in the subjects with clinical lipoatrophy," they wrote in their discussion. "These observations suggest that lipoatrophy does not have an independent effect on endothelial or cardiovascular markers."

But, they added, "The correlation between inflammatory markers and endothelial activation markers in the HIV positive groups suggests that inflammation may play a significant role in endothelial dysfunction seen in HIV."

Intracranial hemorrhage unlikely with tipranavir for HIVAlthough use of the protease inhibitor tipranavir by patients with HIV might prompt an increase in the risk of intracranial hemorrhage, such events are rare, researchers report in the November 1st issue of Clinical Infectious Diseases.

Dr. David Farrar (right) led immunology researchers, including student assistants Ann Davis (center) and Hilario Ramos, in demonstrating that the protein interferon plays a key role in "teaching" the immune system how to stave off repeated infections of the same virus. (Credit: UT Southwestern Medical Center)

ScienceDaily (Dec. 8, 2008) — Scientists at UT Southwestern Medical Center have determined that the immune-system protein interferon plays a key role in "teaching" the immune system how to fight off repeated infections of the same virus.The findings have potential application in the development of more effective vaccines and anti-viral therapies.

Typically, when a person is infected with a virus, the human body immediately generates a massive number of T cells – a type of immune cell – that kill off the infected cells. Once the infection has cleared, most of the T cells also die off, leaving behind a small pool of central memory cells that "remember" how to fight that particular type of virus if the person is infected again.

"In this study, we have uncovered interferon's role and the key signaling protein, called IL-2, involved in generating memory T cells," said Dr. David Farrar, assistant professor of immunology at UT Southwestern and senior author of the study. "Knowing how T cells acquire this memory may help us design better strategies and vaccines to fight HIV and other infectious diseases. Further, our discovery was made using primary human CD4+ T cells, which underscores the relevance of our discovery to human immune responses."

CD4+ T cells coordinate the actions of other cells at the site of infection.

When a virus or bacterium infects a human, the infected cells secrete several molecules, including a cytokine – or signaling protein – called interferon alpha. The action of interferon is what makes an infected person feel run down and tired. Although scientists knew that interferon alpha prevented a virus from multiplying and spreading, they didn't know what role interferon played in the creation of memory cells.

In the current study, the UT Southwestern researchers show that both interferon alpha and another signaling protein called IL-12 are needed to induce the creation of memory cells. They found that interferon and IL-12 team up to promote the creation of a special set of cells that then secrete another signaling protein called IL-2. These IL-2-secreting cells are the ones that remain in the body and "remember" how to fight off the virus.

"Without the IL-2 signaling protein, you'll generate a beautiful primary response against a virus, and you'll eliminate the bug, but your body won't remember how it defeated the virus," Dr. Farrar said. "Without these memory cells, your body is defenseless against re-infections."

Ann Davis, student research assistant in immunology and lead author of the study, said this suggests a new role for interferon: teacher.

"This is really the first demonstration of a role for interferon in teaching a T cell how to respond to viral infections," she said.

Dr. Farrar added: "Up until now, interferon has always been appreciated for its role in inhibiting virus infections. But no one's really paid attention to interferon and its role in regulating memory. That's why we're so excited about this result."

The next step, Dr. Farrar said, is to complete the same study in mice. Early results show that mice with T cells that can't respond to interferon are unable to protect themselves when a virus invades.

"Their immune systems have no idea how to fight the virus," Dr. Farrar said. Dr. Farrar said these early findings in mice may pave the way for designing more effective vaccines.

This research is available online and in the Dec. 15 issue of the Journal of Immunology. Other UT Southwestern researchers involved in the study were Hilario Ramos, student research assistant in immunology, and Dr. Laurie Davis, associate professor of internal medicine.

Current FDA leaders “have lined their pockets,” Obama told A leading US politician has told President-elect Barack Obama that “a complete change” is needed in the leadership of the Food and Drug Administration, as the agency’s current senior staff are “too close with the industries they regulate, creating a question of whom they are working for.”

“I would encourage you not to appoint any current senior FDA employee as Commissioner or Interim Commissioner of the FDA,” writes Bart Stupak, the Democratic Representative for Michigan, in a letter to Mr Obama released last Friday. While he names no agency officials in his letter, Rep Stupak’s plea to the incoming president is being widely seen as an attempt to counter support for Dr Janet Woodcock, head of the agency’s Center for Drug Evaluation and Research (CDER), to be the next Commissioner, or to take the post on an interim basis, when Dr Andrew von Eschenbach steps down.

Commissioner von Eschenbach, who has held the post since September 2005, has made no announcement about his future plans, but his resignation is expected shortly.

Rep Stupak has been a member of the House Energy and Commerce Committee for 12 years, during which time he has been involved in “numerous” investigations of the FDA, he tells Mr Obama. Also, for the past two years has chaired the panel’s oversight and investigations subcommittee, which has primary oversight of the FDA, and: “since February 2007, I have held 16 hearings into the inadequacies of the FDA to protect Americans from unsafe food, drugs and medical devices. The subcommittee’s investigations revealed how the current FDA senior management blocked clinical trials, drove dedicated medical professionals out of the agency and lined their pockets with outrageous bonuses. The agency has abandoned its core mission of protecting Americans from contaminated food, unsafe drugs and medical devices,” he writes.

“A new Commissioner or Interim Commissioner must bring the agency back to the forefront of science, integrity and transparency,” Rep Stupak urges the incoming president.

CDER director Dr Woodcock is widely reported to be the industry’s choice to lead the Administration. This fact alone could be enough to wreck her chances of landing the post, and her 22 years at the agency also means that she is not regarded as a likely force for reform.

Pfizer whistleblower says: "I want to be FDA Commissioner"

Meantime, a new name in the frame for FDA Commissioner is Peter Rost, the controversial former Pfizer vice president who is currently involved in long-running whistleblower litigation against his former employer. He has made public his interest in the agency top job and is being supported by Democrat Sherrod Brown, the junior Senator from Ohio, with whom he has campaigned for imports of cheaper prescription drugs from Canada, and by Missouri Democrat Representative Jo Ann Emerson. Rep Stupak is also reported to be backing Mr Rost.

Combination therapies similar to those used for HIV patients may be the best way of treating hepatitis C virus (HCV), say researchers from the University of Leeds.

A study of a protein called p7, has revealed that differences in the genetic coding of the protein between virus strains - known as genotypes - alter the sensitivity of the virus to drugs that block its function. Read New treatment therapy helps inhibit hepatitis C

The p7 protein assists the spread of HCV around the body and is a promising target for new drug treatments for the virus. Its role was discovered in 2003 by Dr Steve Griffin with Professors Mark Harris and Dave Rowlands of the University's Faculty of Biological Sciences. In laboratory tests their latest research shows that inhibiting p7 with drugs can prevent the spread of HCV..

"One of the challenges in finding treatments for viruses is their ability to constantly change their genetic makeup," says Professor Harris. "Our research shows there can't be a one-size-fits-all approach to treating HCV with p7 inhibitors in the future. We believe combination treatments will work much more efficiently, as they take into account the variability of the p7 protein."

Approximately 180 million people worldwide are infected by HCV, which causes inflammation of the liver and can lead to liver failure or liver cancer. Spread by contact with infected blood or other bodily fluids, there is no vaccine against the disease which is largely asymptomatic in its early stages. The disease is currently treated with broad spectrum, non-specific anti-viral drugs.

Dr Griffin and Prof. Harris examined the response of HCV to a panel of compounds including the well known anti-viral drug, rimantadine, which targets a similar protein in the flu virus. They found that the drug's effectiveness was altered depending on the genetic makeup of the p7 protein.

"We 'borrowed' rimantadine to test its effects because p7 behaves similarly to a protein found in the flu virus," says Dr Griffin. " Although rimantadine works well in the laboratory, we now need to develop new drugs specifically targeted against p7 that we can take forward for future therapies."-University of Leeds

ROCKVILLE, Md., Dec. 8 /PRNewswire-FirstCall/ -- Human Genome Sciences, Inc. (Nasdaq: HGSI - News) today announced that Albuferon® (albinterferon alfa-2b) met its primary endpoint of non-inferiority to peginterferon alfa-2a (Pegasys) in ACHIEVE 2/3, a Phase 3 clinical trial of Albuferon in combination with ribavirin in treatment-naive patients with genotypes 2 and 3 chronic hepatitis C (p=0.0086). Albinterferon alfa-2b is being developed by HGS and Novartis under an exclusive worldwide co-development and commercialization agreement entered into in June 2006.

"We are pleased that Albuferon met its primary endpoint in the ACHIEVE 2/3 trial. These Phase 3 data show that the efficacy of Albuferon was comparable to Pegasys, with half the injections," said H. Thomas Watkins, President and Chief Executive Officer, HGS. "We look forward to having the results of ACHIEVE 1, our other Phase 3 trial of Albuferon, in March 2009. If ACHIEVE 1 is successful, we believe Albuferon could become the market-leading interferon for the treatment of chronic hepatitis C, and we expect that global marketing applications will be filed by fall 2009."

In one presentation, the Italian Cooperative Study Group in a phase II study investigated the use of single dose Zevalin as sole initial treatment in 15 patients with advanced stage (III-IV) follicular NHL. Ninety-three percent (93%) of patients had a response with 73% achieving a complete remission (CR). At a median follow-up of 10 months, 93% of patients are alive, with 71% in continuous CR. No patients required hematopoietic growth factors. Hematologic toxicity was low and quickly reversible; 7 patients developed grade 3 thrombocytopenia and 5 required platelet transfusions.

In a second presentation, investigators from the European Institute of Oncology, Milan treated 13 patients with relapsed or refractory primary gastric NHL including 9 patients with Mucosa Associated Lymphoid Tissue or MALT with a single dose of Zevalin. Ten of 13 patients achieved a CR with all 9 patients (100%) with MALT achieving a CR. Toxicities were mainly hematologic and reversible. After a median follow up of 36 months 9 of 10 CR's (90%) are disease free.

The potential benefits of RIT with Zevalin combined with BEAM conditioning regimen (Z-BEAM) followed by autologous stem cell transplantation (ASCT) for patients who fail to achieve a CR after front line rituximab containing multi- agent chemotherapy for advanced NHL was also presented. The results of the Italian Multicenter Study demonstrated that among 53 patients who failed to achieve CR after CHOP-R, the Z-BEAM followed by ASCT resulted in a 74% CR rate. At a median follow up of 175 days post transplant 40 patients (75%) are alive, 30 patients (57%) in CR. Fourteen patients died, 7 due to treatment related toxicities, and 6 due to progressive disease. The estimated 3 year event free survival (EFS) 64%

"These three additional studies add to the growing body of clinical trial evidence that radio-immunotherapy with Zevalin produces high, durable rates of complete remission in high risk, relapsed or refractory NHL," noted Jack Singer, M.D. and Chief Medical Officer of CTI. "We believe that the impressive 73% CR rate when given as a single agent in previously untreated patients with follicular NHL is worth pursuing in additional trials as it could potentially provide an alternative to multiagent chemotherapy regimens particularly among elderly or infirm patients. Similarly, the 100% CR rate in MALT is an intriguing finding that could represent an additional registration route as it is an unmet medical need. We believe with these and additional prospective randomized clinical trials Zevalin, Radio-Immunotherapy, may finally assume a role alongside cornerstone treatment regimens for NHL," Dr. Singer added.

About Zevalin(R)

Zevalin(R) (Ibritumomab Tiuxetan) is a form of cancer therapy called radioimmunotherapy and is indicated as part of the Zevalin therapeutic regimen for treatment of relapsed or refractory, low-grade or follicular B-cell non- Hodgkin's lymphoma, including patients with rituximab refractory follicular NHL. Zevalin is also indicated, under accelerated approval, for the treatment of relapsed or refractory, rituximab-naÃ¯ve, low-grade and follicular NHL based on studies using a surrogate endpoint of overall response rate. It was approved by the FDA in February of 2002 as the first radioimmunotherapeutic agent for the treatment of NHL.

Rare deaths associated with an infusion reaction symptom complex have occurred within 24 hours of rituximab (Rituxan(R)) infusions. Yttrium-90 Zevalin administration results in severe and prolonged cytopenias in most patients. Severe cutaneous and mucocutaneous reactions have been reported. The most serious adverse reactions of the Zevalin therapeutic regimen were primarily hematologic, including neutropenia, thrombocytopenia and anemia. Infusion-related toxicities were associated with pre-administration of rituximab. The risk of hematologic toxicity correlated with the degree of bone marrow involvement prior to Zevalin therapy. Myelodysplasia or acute myelogenous leukemia was observed in 2 percent of patients (8 to 34 months after treatment). Zevalin should only be used by health care professionals qualified by training and experience in the safe use of radionuclides.

Adherence with Lopinavir/ritonavir (LPV/r) Tablet and Soft-Gel Capsule (SGC)-Based Antiretroviral Regimens and Predictors of Early Treatment Compliance During the first 12 weeks of randomized therapy, LPV/r QD dosing resulted in higher levels of adherence than BID dosing.In the setting of this clinical trial, adherence to LPV/r tablets and SGC was similar. Of note, because MEMS caps were used, subjects were required to dose LPV/r from the original container which could have impacted potential differences in adherence related to the convenience of the LPV/r tablet.Sex, age and race were predictors of early adherence.Differences in early adherence at 12 weeks do not appear to predict clinical outcomes at 48 weeks.The significant between-strata difference observed in CD4+ T-cell increases when comparing whites to non-whites was consistent over time and may, in part, reflect the baseline CD4+ T-cell count difference between whites and non-whites observed in this study.

Metabolic Evaluation of Study M05-730 through Week (Wk) 48In this study of antiretroviral-naïve HIV-infected subjects starting a LPV/r-based antiretroviral regimen:There were increases in all lipid parameters through 48 weeks, including HDL levels. Importantly, however:Median lipid values for TC, TG, and LDL stayed within the acceptable NCEP or clinically relevant values through 48 weeks. This was reflected by the fact that if subjects came into the study with an acceptable TG level at BL (< 2.825 mmol/L), 80% maintained these levels at Wk 48. Also, if subjects came into the study with an acceptable TC level at BL (< 5.2 mmol/L), 72% maintained these levels at Wk 48. In addition, if subjects came into the study with an acceptable LDL level at BL (< 3.38 mmol/L), 87% maintained these levels at Wk 48.The proportion of subjects with low HDL (<1.04 mmol/L) by NCEP decreased from 60% to 33% from BL to Wk 48....

DOUBLING THE DOSE OF RALTEGRAVIR (RAL) DOES NOT INCREASE TROUGH LEVELS IN THE PRESENCE OF RIFAMPIN (RIF)Coadministration of 800mg q12hr RAL with 600mg qd RIF is generally well-tolerated.Although doubling the RAL dose to 800 mg q12hr when coadministered with RIF compensates for the effect of RIF on RAL exposure (AUC0-12hr), it does not overcome the effect of RIF on RAL trough concentrations (C12hr).Trough concentrations remain above the protein- adjusted IC95 (31nM).The decrease in C12hr is similar to what is seen with coadministration of 400 mg q12hr RAL and RIF.Although trough concentrations have not been shown to correlate with efficacy, caution should be used when RAL is coadministered with RIF until additional clinical information is available.

Omeprazole Increases Plasma Levels of Raltegravir (RAL) in Healthy SubjectsOmeprazole increases plasma concentration of RAL in healthy subjectsPopulation PK data demonstrate that patients with HIV infection receiving RAL have similar RAL levels whether or not they receive PPI or H2 blockersReported differences in gastric pH between HIV infected patients vs uninfected subjects may explain this dichotomous findingRAL codosed with omeprazole or other pH-altering agents is generally well-tolerated and no areas of concern have been identifiedData support use of RAL with gastric pH-altering agents with no dose adjustment Further investigation is necessary to more fully characterize the PK of RAL given in combination with pH-altering agents in HIV-infected patients

Raltegravir (RAL) Pharmacokinetics in Individuals with UGT1A1*1/*1 and UGT1A1*28/*28 GenotypesRAL is generally well tolerated in individuals with UGT1A1 *28/*28 and UGT1A1 *1/*1 genotypes.Plasma concentrations of RAL are modestly higher in individuals with the UGT1A1 *28/*28 genotype relative to the UGT1A1 *1/*1 genotype.The difference in the pharmacokinetic profiles in the 2 groups is not considered to be clinically meaningful.Overall clinical experience with RAL indicate that exposure increases on the order of 2-fold are not associated with increased risk of toxicity.No dose adjustment of RAL is required for individuals with the UGT1A1*28/*28 genotype

Possible AIDS Treatment Shows Promise in MonkeysWEDNESDAY, Dec. 10 (HealthDay News) -- Researchers report that a treatment under development appears to stop the equivalent of the AIDS virus in monkeys.

Nine rhesus macaque monkeys infected with a virus known as SIV underwent treatment and remain alive eight months later. The treatment appears to work by preventing virus cells from fooling the immune system.

There's no guarantee that the treatment will work in people. But if it's effective in humans, the treatment could allow patients to avoid taking AIDS drugs for the rest of their lives, said study co-author Rama Rao Amara, an assistant professor at Emory University's Yerkes National Primate Research Center.

"If you wake up and realize you don't have to take a pill, it's a big step forward," he said. In addition, he said, current AIDS drugs are expensive and have serious side effects.

Existing AIDS drugs do have benefits: They're often effective and have allowed patients to live normal lives. However, they can't always keep up with the AIDS virus, which evolves quickly and can become immune to current treatments.

"The virus changes and then these drugs don't work after some time," Amara said.

In the new study, Amara and colleagues injected nine monkeys with an antibody that blocks a kind of "don't kill me" signal that cells infected with simian immunodeficiency virus (SIV) send to immune cells.

When the SIV-infected cells emit the signal, "the killer cell thinks, 'You are not my enemy. You're my friend,'" Amara said. But when the signal is blocked, the killer immune cells can do their job and wipe out the virus.

The researchers gave four injections of the antibody to the monkeys over 10 days and then watched to see what happened.

The study appears in the Dec. 10 online edition of Nature

The monkeys, infected with SIV for as long as 21 months, were able to beat back the virus. Levels of virus in the blood dropped and the animals remained alive.

By contrast, four out of five monkeys who received a "control" antibody died within four months.

"What is amazing to me how rapidly you can actually change these killer cells," Amara said. "Now they are good cells."

The work of the monkeys is done and they will be euthanized, Amara said. It is too expensive -- $7 a day each -- to pay for their care with available funding, he said.

In humans, the treatment could cost a couple thousand dollars per dose, Amara said, although patients might then avoid taking drugs for life.

Dr. Mark Connors, a specialist in AIDS research, said the research is "clearly valid and very interesting. I'm sure it's going to generate debate over the next year or so as to what it means."

Even skeptics may be convinced by evidence that the treatment directly affects survival and the level of the virus in the body, said Connors, chief of the HIV-Specific Immunity Section at the U.S. National Institute of Allergy and amp; Infectious Diseases.

As for the future, Connors said he's "guardedly optimistic" that the treatment could be used in humans, perhaps in conjunction with other medications.

The HIV transmission rate in the U.S. has decreased by 89% since 1984 and 33% since 1997CDC in a research letter published in the Journal of Acquired Immune Deficiency Syndromes released updated estimates of HIV transmission rates in the U.S., Reuters reports. According to the letter -- written by researchers from CDC and Johns Hopkins University -- the HIV transmission rate in the U.S. has decreased by 89% since 1984 and 33% since 1997. In addition, about 5% or less of people living with the virus will transmit it to another person in any given year, according to the letter (Fox, Reuters, 12/9). The study also found that in 1984, there were 44 transmissions per 100 people with HIV. By 2006, there were just under five transmissions per 100 HIV-positive people (CDC fact sheet, December 2008). David Holtgrave, a researcher at Johns Hopkins who led the study, said, "For every 100 persons living with HIV today, five or fewer will transmit the virus to an uninfected person in a given year."

Richard Woltiski of CDC said the declining transmission figures "really show that people living with HIV are taking steps to be responsible and protect others" and "reflect the success of prevention efforts across the nation." He added that the decreasing transmission rate is most likely the result of a "combination" of HIV prevention efforts that include "HIV testing, prevention programs for people who are living with HIV and those who are at risk for HIV, as well as the effects of HIV treatment that have prolonged the lives of so many people living with HIV." The study was based on the latest CDC data on HIV/AIDS in the U.S. The agency in October announced that 1.1 million people are living with HIV in the U.S., and in August it announced that 56,300 new infections occur annually.

Woltiski said even with the "success" in lower transmission rates, "we cannot forget that new HIV infections are increasing among" men who have sex with men and that "African-Americans and Hispanics continue to experience disproportionate and unacceptably high rates of HIV and AIDS. The fight against HIV is far from over" (Reuters, 12/9).

A CDC fact sheet about HIV transmission rates is available online (.pdf). A Johns Hopkins press release about the study also is available online .